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Originally Posted by energyperson I am interested to know if depression can be healed by using self help exercises? |
Some words and links that might assist you. Do keep in mind your situation of depression is not a simple thing to cope with. Many variable come into play, and if not recognized, just doesn't get the job properly corrected.
You are a spirit, soul and body, and ignoring any one of them, while addressing any difficulty, just won't correct the way you are currently feeling.
Am offering, from a lay persons point of view, things that might help you or others. Not a doctor, nor do I pretend to be qualified enough to positively say do this, or that, and you will be cured. Use of EFT (info on my blog also) might be a real help. There are a couple good suggestions already posted here in this topic.
Be well.
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Lithium: How Good is it? Interview with Dr. H. ManjiPsychEducation.org
Lithium: How Good is it?
Many people worry that lithium is one of psychiatry's "Big Guns", something
we use for patients with really severe mental illnesses. They think, "Hey, I'm
not that sick", and conclude that lithium is not right for them.
They don't know that lithium, in lower doses, is used in plain depression (not
bipolar, not severe). In fact, for depression that hasn't fully responded to an
antidepressant, one research group calls it "Step 1A" -- the thing to do, in
some cases, before switching to another antidepressant.
But one of the strongest arguments for lithium is the way it appears to protect neurons. So I wanted to show you the world's expert on how lithium works, talking about this aspect of lithium's potential benefits. His full comments, on a range of topics, from his interview with a great bipolar advocacy organization, can be read on this link at the Child and Adolescent Bipolar Foundation (CABF).
Here are Dr. Manji's comments about lithium (it's a little technical; look for
the few ideas I put in bold if you're getting bogged down):
CABF: Speaking of lithium, your research has uncovered some of its intriguing
beneficial properties. Can you highlight the most important ones?
MANJI: Many of the genes that are considered neuroprotective [keep brain
cells from dying when stressed] are being remarkably turned on by lithium. Is
lithium actually neuroprotective? We hadn't thought this way before. A
number of studies have taken animal cells and tried to kill them by causing
stroke, etc. These studies have consistently shown that lithium, if
administered before you try to do the bad things (such as induce a stroke),
protects the animal's neurons. In lithium-treated brains, the size of the
resulting stroke is smaller, the number of neurons that die is lower, etc. That
was amazing. Since these studies were done in rats, you need to be careful
about jumping to conclusions that lithium is neuroprotective in people.
Wayne Drevets' group published a finding in Nature about five years ago that
in a part of the pre-frontal cortex of bipolar patients or patients with familial
recurring unipolar depression, there was almost a 40% reduction in the
amount of gray matter. That was a remarkable finding that you have such a
reduction in a discrete part of brain. We spoke to him about our lithium
findings and asked him to reanalyze the data. He had a small group of patients who had been treated with lithium for a long time and they did not show the brain atrophy compared with the bipolar patients. Interestingly all of the patients with unipolar depression, whether or not they had been treated with antidepressants, still showed the atrophy. That was a suggestion that bipolar treatments might have a protective effect.
Valproate (Depakote) in the prefrontal cortex seemed to have the same type
of neuroprotective properties. Lithium and depakote do not have identical
effects in every brain area, but in this area they did. Brains treated with
chronic lithium or valproate seemed not to have the atrophy in the prefrontal
cortex.
But it was a very small sample and a crossectional study [type of study whose design restricts its findings to association between variables, not proof of cause]. He studied them once. We don't know if it was a cause or effect. Is it the people who don't have the atrophy who responded to the drug in the first place?
We did some studies taking bipolar patients off their meds -- they were
referred to us because their treatments weren't working. In every case, they
either hadn't been on lithium or had been on lithium sparingly -- had started
on it, had side effects, switched, and the new med was not working. These are bipolar depressed patients. We did MRI scans and MRS spectroscopy and then put them on lithium in a blinded fashion for 4-6 weeks. Then we did the scans again. We found that almost every single person taking lithium had an
increase in N-acetylaspartic acid (NAA) [an amino acid that is viewed as a
marker of neuronal health]. And the actual amount of gray matter was going
up when they were treated chronically with lithium. This study was done
together with Dr. Greg Mooreš. This was happening in areas of the patients'
brains that had been atrophied. The increase was not due to swelling from
water retention. The increase was seen only in areas where the brain matter
had previously atrophied.
Our working hypothesis, and I think it is reasonable, is that lithium is turning
on some of these growth signaling pathways and reversing the damage. It
seems that the cells are shrunken, not dead, and are capable of going back to their normal sizes and sending normal projections. What lithium seems to be doing is turning on the signaling pathways that produce growth factors in the brain, such as brain-derived neurotrophic factor (BDNF), and where you have atrophy, turning on this pathway seems to be capable of reversing it. And that is a remarkable finding.
A couple of other studies since then have compared lithium-treated patients
with untreated patients. They showed that the lithium-treated patients have
the increase in gray matter, suggesting that lithium is causing the increase. If
that is the case, lithium has a neurotrophic [nourishing to neurons] effect.
Would lithium, then, be beneficial in any bipolar patient, even if he or she
can't tolerate it or if his or her symptoms respond better to another mood
stabilizer? One question is tolerability. We've done a number of animal studies
with low-dose lithium. We found that in animals, with a dose of lithium that is
one-half or one-third of a usual dose, you still get a large increase in bcl-2,
a neuroprotective protein. This suggests that it is quite possible that even
low-dose lithium will exert these effects. Many studies are being planned
using low-dose lithium as an additional agent in patients being treated with
something else. We will add low-dose lithium and follow them for 2-3 years
with repeated MRIs and neuropsych testing to see if the addition would be
enough to provide neuroprotective effects that would help them long-term
with the illness, even if something else is their appropriate treatment for
symptoms. That is extremely important. It is a devastating long-term illness,
and brain atrophy may be responsible for that. If we can intervene early on
and prevent that, there is reason to believe you will have a big impact on the
overall course of the illness.
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